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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5191_Библиотеки_им_академика_М_И_Перельмана.pdf
Pressure Necrosis inGeriatric
Patients
JoyceBlack
70
70.1 Background
The elderly remains one of the highest at-risk
populations for pressure ulcers. A systematic
review reported that on average, the incidence of
pressure injury is 12% in all persons [1]. However,
the highest reported rates were in elders with
fractured hips; 70% of them developed pressure
ulcers [2]. The incidence of pressure ulcers in
elderly population varies by care setting, but evidence on risk factors indicates that age will
increase the probability of pressure ulcers, particularly in patients with limited mobility.
Chronic medical conditions are also more prevalent in older adults. Long-term care patients have
the highest rate of PU development associated
with higher frequency of mortality and advanced
severe chronic conditions. The common agerelated chronic diseases are identied as cardiovascular, diabetes, lung, renal, musculoskeletal,
and neurodegenerative diseases. Progression of
these diseases is often seen as impaired motor,
sensory, immune, and hormonal systems and lead
to frailty, disability, geriatric syndromes, and isolation. The signicance of comorbidity risk factors in the pathogenesis of PU requires further
investigation, recognizing the insolvability of PU
prevention solely with external relief devices [3].
J. Black (*)
University of Nebraska Medical Center, College of
Nursing, Omaha, NE, USA
e-mail: jblack@unmc.edu
70.2 Etiology/Pathophysiology
Pressure ulcers are aptly named because they
develop due to pressure. Pressure is a static,
direct compressive force on tissue leading to
hypoxia of the skin and soft tissue by restricting
blood ow. When pressure reaches magnitudes
that deform cells, the resulting injury is classied
today as deep tissue injury, in that the pressure
was applied to the deep tissues (muscle, fascia)
and deformed the cells leading to their death [4,
5]. Pressure of less magnitude and of long dura-
tion creates tissue ischemia. Ischemia of tissue
also leads to necrosis, but the mechanism is due
to depletion of oxygen and glucose and accumulation of lactic acid [6, 7].
The time needed to create ischemia in soft tissue and skin which leads to necrosis is elusive. In
an ischemic animal model, 70% of cell viability
remained for over 22h. In contrast, cell deformation which would lead to deep tissue injury was
evident within the hour [8] (see Fig. 70.1). Of the
various tissues that are at risk of death due to
pressure, muscle tissue is damaged rst, likely
because of its increased need for oxygen and
higher metabolic requirements. By the time
ulceration is visible in the skin, signicant damage of underlying muscle may already have
occurred. The tissue fed by the vertical perforators through the muscle remains viable for a
while; a series of cases showed the rst sign of
skin injury from intense pressure was apparent
48h after the pressure was applied [9]. An addi-
© The Author(s) 2024
L. Téot et al. (eds.), Skin Necrosis, https://doi.org/10.1007/978-3-031-60954-1_70
453
454
Tissue compression
and mechanical
properties
J. Black
Stimulation
Inhibition
Deformation
T
def1
Apoptosis
Ischemia
Fig. 70.1 Model of proposed sequence of events leads to
necrosis of tissue. Deformation of tissue leads to damage
when the threshold is met (T def 1), and cells will start a
programmed cell death leading to necrosis. If the deformation of the cell exceeds its tolerance, the cells will die
Necrosis
Ischemia
T
def2
Metabolic
processes
Ischemia
Ischemia
Ischemia
Ischemia
Oxygen
Lactate
Ischemia
T
lac
Apoptosis ?
Ischemia
immediately from necrosis. Cells can also be injured from
ischemia, reducing the metabolic substrates needed and
leading to anaerobic metabolism and accumulation of lactic acid. Both cellular starvation and acidication lead to
apoptosis and cellular necrosis (From Stekelenburg [10])
Glucose
Ischemia
T
glv
tional nding from this case series is that patients
who sustained deep tissue injury were not aware
of the ischemia; they were unconscious.
Restoration of blood ow to an ischemic area
of tissue, or reperfusion injury, causes more
damage to the injured area, causing a pressure
ulcer to enlarge or fail to heal. Reperfusion of
blood causing cellular edema, tissue damage, and
overproduction of reactive oxygen species trigger
a process termed oxidative stress, which may
cause the accumulation of unfolded proteins in
the endoplasmic reticulum [11].
Shear is also a cause of pressure ulcers and
undermining in existing ulcers. Shear is a tangential
(angular) force associated with movement, for
example, sliding down in bed or being pulled over
to the side of the bed. Shear forces distort blood vessels in the skin, making the effect of pressure more
deleterious because the tissue is already hypoxic.
Research has shown that positioning a patient at 45°
head of bed elevation leads to the most detrimental
combination of pressure and shear on the sacrum,
because the shear stresses combined with pressure
cause greater obstruction and distortion of capillaries in skeletal muscle around bony prominences
than does pressure alone [7].
Microclimate, the moisture and heat of the
skin, increases the risk for pressure ulcers because
70 Pressure Necrosis inGeriatric Patients
455
the moisture macerates the skin. The boggy skin
does not glide against bed sheets and leads to
supercial tissue injury. Skin exposure to urine or
stool also injures the skin and increases risk of
tissue damage from pressure and shear. Gefen
[12] has provided a theoretical explanation of the
ways in which a changing microclimate may
inuence the development of supercial pressure
ulcers. From a mathematical model, Gefen postulated that four microclimate changes may inuence pressure ulcer development—increasing
skin temperature, increasing ambient temperature, increasing relative humidity, and decreasing
the permeability of sheets or clothing.
The tolerance of the skin and soft tissue for
pressure and shear is also crucial to understand
how pressure ulcers develop. Atherosclerosis is a
common disease of the elderly. As the disease
progresses blood ow to distal areas, such as the
lower leg is signicantly reduced. The reduced
perfusion limits the ability of the soft tissue to be
reperfused following a pressure loading event. A
lack of sensation, due to stroke or peripheral neuropathy especially from diabetes creates an
unawareness of pressure on the heel in a bedridden patient. When these comorbid states are
combined with a traumatic event, such as a fall
with hip fracture, the risk is much greater. Heel
ulcer development in hip fracture patients with
underlying diabetes and peripheral vascular disease is not only common, but is also very slow to
heal due to the same processes.
In part due to the chronic conditions, many
patients will experience dysphagia or anorexia
and as a result lose weight. Sarcopenia leads to
decreased strength of the lower extremities,
frailty, and often of immobility. Malnutrition
also impairs immune and hormonal function,
causes skin changes (epidermis, dermis),
reduces subcutaneous tissue, and causes muscle
atrophy, all increasing vulnerability to PU [13].
Finally, urinary and fecal incontinence reduce
the tolerance of skin for pressure and shear as
well as chemically damage the skin. Incontinence
is one of the most common reasons for admission to long-term care. Efforts should be made
to determine the causes such as urinary infection and reduce the continuous exposure to urine
and diarrheal stool.
70.3 Presentation
Pressure necrosis appears on tissue that has been
subjected to intense pressure in patients who cannot feel the pressure or respond to it and change
positions. Pressure ulcers are categorized based
on the amount of visible tissue in the wound bed.
Category/Stage 1: Nonblanchable erythema.
Category/Stage 2: Supercial loss of mid dermis.
Appears bright red if ulcer is in the papillary
dermis and off-white if in the reticular
dermis.
Category/Stage 3: Loss of dermis with exposed
fat when not on a bony prominence.
Granulation tissue present when healing.
Category/Stage 4: Loss of dermis with exposure
of muscle, tendon, bone, cartilage. Granulation
tissue present when healing.
Unstageable: wound bed obscured with slough or
eschar so that true extent of the ulcer cannot
be described. If the ulcer is debrided, it is then
staged.
Deep tissue pressure injury: initially purple or
maroon intact skin. Within 48 h, epidermis
slough occurs, which looks like a broken blister. As the ulcer evolves, it should be classied
as noted above almost all of these wounds are
stage 4.
High-risk patients and the common locations
for pressure necrosis are as follows. It is important to identify the location of the patient at the
time the pressure injury started, so that position is
avoided. Continued pressure on a pressure ulcer
will increase the ischemia in the issue and lead to
signicant deterioration.
456
J. Black
Position
Flat in supine position
(e.g., during surgery,
hypotensive)
Supine with head of bed
elevated 30–45° or
slouching in a chair
Common location of pressure
necrosis
Buttocks tissue, unless patient
is quite thin, with no buttocks
tissue
Necrosis appears bilaterally
Sacrum and adjacent buttocks
tissue
Example pressure necrosis leading to deep tissue
injury
Sitting erect in chair Ischial tuberosities
70 Pressure Necrosis inGeriatric Patients
457
Position
Supine with heels on the
bed
Wearing medical devices
that are tight
Common location of pressure
necrosis
Posterior heel in patients with
immobile legs, neuropathic
legs, or peripheral vascular
disease
Bridge of the nose from
noninvasive positive pressure
masks, behind the ears from
oxygen tubing, shin, top of foot,
and along Achilles tendon from
stockings
Example pressure necrosis leading to deep tissue
injury
70.4 Dierential Diagnosis [14]
• Abscess
• Arterial leg ulcer
• Bruising
• Calciphylaxis
• Cellulitis
• Critical limb ischemia
• Cutaneous malignancy
• Diabetic foot ulcer
• Fournier’s gangrene
• Hematoma/Morel–Lavellée lesions
• Incontinence-associated dermatitis/moistureassociated skin damage
• Ischemia of the skin beneath tightly wrapped
dressings
• Necrotizing fasciitis
• Skin tear
• Venous leg ulcer
• Warfarin-induced necrosis
• Wound dehiscence
70.5 Prevention
Reducing the duration and magnitude of pressure
is paramount. The duration of pressure is reduced
by turning the patient off of high-risk areas. Most
458
ab
J. Black
pressure necrosis develops on the sacrum, and
therefore immobile patients should be turned to
the side to relieve pressure. The frequency of
turning can be every 3h as long as the patient is
on a quality mattress [15]. The magnitude of
pressure can also be reduced by placing the
patient on a support surface with adequate envelopment and immersion. High-density foam mattresses have been shown to be effective in
reducing pressure injury as long as the patient is
moved about in bed. For very high-risk patients,
alternating pressure mattress helps prevent tissue
damage; however, the patient still must be moved
on these support surfaces. No support surface
replaces turning the patient to reduce duration of
pressure. Use mattress of 4inches (10cm) of viscoelastic foam during times when patients cannot
be moved, such as surgical cases over 3h cardiopulmonary bypass cases, and in the emergency
department [16]. For bedbound patients, the use
of signaling devices to notify staff when the
patient should be turned have been shown to
reduce pressure injury rates [17]. Turn teams
have also been able to reduce pressure injury
rates [18].
Heels should be elevated from the bed in highrisk patients. Heel elevation can be done with a
pillow placed under the calf of the leg in order to
“oat” the heel from the bed. Pressure-relieving
boots can be used when patients do not stay in
place on pillows; however, boots themselves can
create pressure points. Therefore, boots need to
be removed 2–3 times daily to assess for early
signs of pressure injury.
Medical devices should be removed 2–3 times
a day, if only long enough to inspect for signs of
pressure on the skin [19]. High-risk areas, such as
the bridge of the nose and face, should be padded
with thin foam dressings prior to the use of noninvasive positive pressure masks [20]. Oxygen
tubing should be padded to reduce the intensity
of pressure behind the ear.
Multilayer foam dressings have been shown to
reduce sacral and heel pressure injury in the critically ill patient, the general hospitalized patient,
and even patients in long-term care. These dressings can reduce the intensity of pressure and
shear on the soft tissues [18].
Nutrition is paramount to prevent pressure
injury. Patients who are catabolic cannot repair
injured tissue. In addition, the lack of subcutaneous tissue in frail patients places more body areas
at risk for pressure injury [13].
70.6 Treatment
Pressure necrosis of the sacrum, buttocks, and
ischia will need debridement to viable tissue if
healing is the goal for the patient (Fig. 70.2a, b).
During the healing process, pressure on the
wound must be limited to 1h 3 times a day (for
Fig. 70.2 (a) This patient is a 65-year-old male who
refused to move from his bed at home for several days.
When admitted to the hospital, he was septic. Cellulitis
and frank necrosis are visible on the sacrum and buttocks.
(b) His wound was debrided at bedside in the ICU due to
the wound being the cause of the sepsis
70 Pressure Necrosis inGeriatric Patients
459
meals). Caution must be used to avoid placing
patients in chairs for multiple hours at a time.
Nutrition must also be adequate to promote healing and reduce the risk of infection. Biolm
quickly develops in these wounds, so debridement is needed along with biolm-resistant
antiseptics should be used (silver, cadexomer
iodine, honey, polyhexanide) [21]. An excellent
review of biolm is provided by Vererosa [22].
Pressure necrosis of the heel should not be
debrided in patients with ischemic limbs. As long
as the eschar remains stable, local wound care
with topical iodine is recommended. The eschar
will lift from the edges and should be trimmed to
prevent it from snagging on clothing. If the eschar
cap is removed from the wound, or the eschar cap
is softened, infection rapidly develops. The poor
inherent blood ow in the limb reduces the likelihood of healing and often leads to amputation
due to critical limb ischemia [14].
Pressure ulcers from medical devices continue
to occur. They are due to several factors: the plastic used to create the device is rm, the sizes are
limited and often need to be forced to t, the
devices are monitoring life altering disease and
cannot be moved, the device is providing lifesaving treatment and cannot be moved. However,
many medical devices can and should be removed
or moved twice daily, to inspect the skin and pad
the skin beneath the device.
The use of bundles of care has improved pressure injury rates for many facilities. The National
Pressure Injury Advisory Panel has created a
bundle for the critically ill. Others are being
developed.
References
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2. Donnelly J, Winder J, Kernohan W, Stevenson M.An
RCT to determine the effect of a heel elevation device
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s12877- 018- 0997- 7.
4. Gefen A.The etiology of pressure injuries. In: Emily
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9. Black JM, Brindle CT, Honaker J.Deep tissue injury:
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Arch Phys Med Rehabil. 2008;89:1411.
11. Tsuji S, Ichioka S, Sekiya N, Nakatsuka T.Analysis
of ischemia-reperfusion injury in a microcirculatory model of pressure ulcers. Wound Repair Regen.
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12. Gefen A.How do microclimate factors affect the risk
for supercial pressure ulcers: a mathematical modeling study. J Tissue Viability. 2011;20(3):81–8.
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Haesler E. The role of nutrition for pressure injury
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Datta S, Colon-Emeric C. TEAM-UP for quality: a
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L, Whitty JA, McInnes E, Lockwood I, Chaboyer
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Deep Dissecting Haematoma:
AFrequent Cause ofNecrosis
inElderly Patient
HesterColboc andSylvieMeaume
71
Deep dissecting haematomas (DDH) are the
result of bleeding, either spontaneous or following trauma [1, 2]. This collection of blood forms
between the hypodermis and the muscular fascia
[1–3], causing a dissection between these two
subcutaneous layers. This dissection deprives the
areas concerned of their blood supply and causes
necrosis of the skin of the top of the haematoma.
lt can be very voluminous and, in extreme
cases, can have hemodynamic consequences that
can even lead to death if the patient is not treated
quickly and appropriately [4].
DDH are diagnosed clinically, but sometimes
require at least a blood test to check for anaemia
if the haematoma is large, and a standard X-ray to
rule out an associated fracture in the event of a
fall or trauma.
71.1 Pathophysiology
DDH is a little-known pathology, which has
mainly been described in elderly people suffering
from dermatoporosis and/or on anticoagulant or
antiplatelet therapy (present in more than half of
the patients concerned) [1, 2, 5].
The term dermatoporosis, by analogy with
osteoporosis, was proposed by Saurat and Kaya
H. Colboc (*) · S. Meaume
Geriatric and Wound Care Department, Rothschild
University Hospital, Assistance Publique Hôpitaux de
Paris, Sorbonne Université, Paris, France
e-mail: hester.colboc@aphp.fr
in 2007 to dene all the manifestations associated with skin ageing, leading to fragility and
skin insufciency [6]. It is characterised by a
structural change in the skin, caused by a reduction in collagen and hyaluronic acid and the
absence of the CD44 glycoprotein (differentiation cluster 44), which is usually present [7].
Traditionally, a distinction is made between two
forms: primary and secondary [8].
The most common form is primary, combining intrinsic factors such as skin aging and extrinsic factors such as chronic sun exposure [9].
The secondary form is iatrogenic due to longterm treatment with topical and/or systemic corticosteroids [10].
There were no signicant clinical differences
between the two types of dermatoporosis.
Clinically, there are four progressive stages of
dermatoporosis [3, 11–13]:
• Stage 1: thin skin, nearly translucent, reveal-
ing a prominence of the underlying veins and
tendons, senile purpura (Bateman purpura)
(Fig.71.1a) and white pseudo scar classically
describe as having a stellate conguration but
can might be also linear or plaque-like
(Fig.71.1b) [1, 12, 14].
• Stage 2: manifestations of stage 1 and small,
localised skin laceration resulting from a
© The Author(s) 2024
L. Téot et al. (eds.), Skin Necrosis, https://doi.org/10.1007/978-3-031-60954-1_71
461
462
H. Colboc and S. Meaume
a
b
cd
Fig. 71.1 Somes clinical aspect of dermatoporosis. (a)
Bateman purpura characterized by hemorrhagic areas
with conuent ecchymoses. (b) Typical aspect of derma-
torosis: white stellar scar, fragile skin and Bateman purpura. (c) Small skin tear or laceration. (d) Large skin tear
cleavage between the dermis and the epidermis (Fig.71.1c).
• Stage 3: more numerous and larger skin lacerations (Fig.71.1d) with a signicant delay
in healing [15].
• Stage 4: progression of the lesions described
above leads to the formation of DDH which
may progress to skin necrosis [1, 12].
71.2 Epidemiology
The incidence of DDH is not well known.
An initial retrospective study, carried out in
2009 on 34 patients, revealed an average age of
81.7 years, with a predominance of women (5
women to 1 man) and advanced dermatoporosis
in all patients [1].
Another prospective study was carried out in
the geriatrics department. Out of 202 patients
aged over 60, signs of dermatoporosis were present in 32% of hospitalised patients. There was a
signicant association (p<0.05) with haematomas of the lower limbs, although the dissecting
nature was not specied [16].
71.3 Clinical Signs
DDH is most often localised to the lower limbs
[1, 3]. More rarely, it may be found on the face
(forehead), occiput, trunk, or upper limbs [2].
lt is manifested by aspecic clinical signs such
as intense pain, and/or tension, and/or swelling,
and/or erythema, which can lead to misdiagnosis.
However, fever is not one of the clinical signs of